Title: Deficit of Kcnma1 mRNA expression in the dentate gyrus of epileptic rats.

Authors: Boris Ermolinsky, Massoud F Arshadmansab, Luis F Pacheco Otalora, Masoud M Zarei, Emilio R Garrido-Sanabria

Journal, date & volume: Neuroreport, 2008 Aug 27 , 19, 1291-4

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/18695509

Abstract
Epileptogenesis in mesial temporal lobe epilepsy is determined by several factors including abnormalities in the expression and function of ion channels. Here, we report a long-lasting deficit in gene expression of Kcnma1 coding for the large-conductance calcium-activated potassium (BK, MaxiK) channel alpha-subunits after pilocarpine-induced status epilepticus. By using comparative real-time PCR, Taqman gene expression assays, and the delta-delta comparative threshold method we detected a significant reduction in Kcnma1 expression in microdissected dentate gyrus at different intervals after status epilepticus (24 h, 10 days, 1 month, and more than 2 months). BK channels are key regulators of neuronal excitability and transmitter release. Hence, defective Kcnma1 expression may play a critical role in the pathogenesis of mesial temporal lobe epilepsy.